Transcriptome analyses and virus induced gene silencing identify genes in the Rpp4-mediated Asian soybean rust resistance pathway.

Rpp4 (Resistance to Phakopsora pachyrhizi 4) confers resistance to Phakopsora pachyrhizi Sydow, the causal agent of Asian soybean rust (ASR). By combining expression profiling and virus induced gene silencing (VIGS), we are developing a genetic framework for Rpp4-mediated resistance. We measured gene expression in mock-inoculated and P. pachyrhizi-infected leaves of resistant soybean accession PI459025B (Rpp4) and the susceptible cultivar (Williams 82) across a 12-day time course. Unexpectedly, two biphasic responses were identified. In the incompatible reaction, genes induced at 12h after infection (hai) were not differentially expressed at 24 hai, but were induced at 72 hai. In contrast, genes repressed at 12 hai were not differentially expressed from 24 to 144 hai, but were repressed 216 hai and later. To differentiate between basal and resistance-gene (R-gene) mediated defence responses, we compared gene expression in Rpp4-silenced and empty vector-treated PI459025B plants 14 days after infection (dai) with P. pachyrhizi. This identified genes, including transcription factors, whose differential expression is dependent upon Rpp4. To identify differentially expressed genes conserved across multiple P. pachyrhizi resistance pathways, Rpp4 expression datasets were compared with microarray data previously generated for Rpp2 and Rpp3-mediated defence responses. Fourteen transcription factors common to all resistant and susceptible responses were identified, as well as fourteen transcription factors unique to R-gene-mediated resistance responses. These genes are targets for future P. pachyrhizi resistance research.

Cerebral blood volume changes during exchange transfusions in infants born at or near term.

We investigated the effects on cerebral hemodynamics of blood pressure changes during exchange transfusions in infants born at or near term, using near infrared spectroscopy in eight stable infants (mean gestational age, 36.2 +/- 1.3 weeks) who underwent a total of 21 exchange transfusions for erythroblastosis fetalis (rhesus hemolytic disease). Changes in mean arterial blood pressure derived from an indwelling umbilical arterial catheter, transcutaneous arterial oxygen and carbon dioxide tension, as well as changes in cerebral oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (HbR), and total hemoglobin (Hbtot = HbO2 + HbR), were recorded continuously from 15 minutes before until the completion of the exchange transfusion. Relative change(s) in cerebral blood volume (dCBV) were calculated as follows: dCBV = change in Hbtot x 0.89/Venous hemoglobin. Changes in mean arterial blood pressure and dCBV were observed during all exchange transfusions; a decrease was found during the withdrawal period and an increase during the infusion period. The mean response of dCBV to a change in mean arterial blood pressure was 0.011 ml.100 gm-1.mm Hg. Multivariate analysis showed that dCBV were primarily associated with changes in mean arterial blood pressure, followed by changes in arterial oxygen tension and in exchange cycle duration. We conclude that in stable term and near-term infants, hemorrhagically induced blood pressure changes provoke dCBV.

Indomethacin-induced changes in renal blood flow velocity waveform in premature infants investigated with color Doppler imaging.

Renal dysfunction has been recognized as an adverse effect of indomethacin treatment and is probably secondary to impairment of renal blood flow. We therefore evaluated renal artery blood flow velocity in 15 premature infants with a symptomatic ductus arteriosus before and during the first 12 hours after a single intravenous dose of 0.1 mg/kg of indomethacin. Renal artery blood flow velocity was measured serially by color-Doppler flow imaging and used as a qualitative measure of true renal blood flow. Indomethacin administration led to a sharp decrease in peak systolic flow velocity and temporal mean flow velocity of the renal artery. This effect was maximal at 10 minutes after indomethacin dosing; the flow velocities showed a slow recovery, reaching baseline values again at 2 hours after indomethacin dosing. We conclude that indomethacin can affect renal blood supply in the premature infant for a period of at least 1 hour after indomethacin treatment.